tag:blogger.com,1999:blog-1442827238174603755.post8261469155301293921..comments2023-09-11T08:30:08.843-07:00Comments on Life Training Institute Blog: Does a Thin Uterine Lining Support the "Pill as Baby Killer" Theory? [Serge]SKhttp://www.blogger.com/profile/01905606527143286458noreply@blogger.comBlogger34125tag:blogger.com,1999:blog-1442827238174603755.post-20314951845135400322017-02-06T11:34:59.974-08:002017-02-06T11:34:59.974-08:00Thank you all for a well-informed resource on this...Thank you all for a well-informed resource on this subject!Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-53179464898893781962015-11-07T02:22:41.430-08:002015-11-07T02:22:41.430-08:00I am so glad I came across this blog, I have found...I am so glad I came across this blog, I have found the debate very enlightening and love that people are being civil and sharing thoughtful, researched viewpoints. This includes your input Anon, however I feel I must point out an error in one of your statements:<br /><br />"They can (and do) experiment with animals in ways not possible with humans, that is, they can apply the hormones, then slaughter the animals and measure the organs. (The experiment we did with mice, with estrogen, progesterone, and both, was such an experiment.)"<br /><br /> The claim that this type of experimentation with humans is "not possible" is incorrect. Technically it IS possible to subject a human being to this type of experimentation, it just would be legally be condoned as torture and subsequently murder and the 'scientist' sentenced to prison assuming they were tried and convicted.<br /><br />I do not wish to interrupt this blog with off topic discussion , however being that the statement was put out there, I feel it is a good opportunity to clarify that there is a difference between what is possible (or not), what is legal, and what is morally/ethically right. They do not always correlate nor are they synonymous with each other.<br /><br />Whether they correlate or not depends on an individual's moral compass, which in turn depends on several, personal factors.<br /><br />Sorry if I seem to be losing my point (I sometimes find it difficult to conclude things) . The point I am trying to make is: I do appreciate the relevant information in your post rereading estrogen and progesterone and do feel you have a unique viewpoint that we can learn from. However, your valuable information was distracted from by your seemingly biased toward animal experimentation, which not everyone shares. I think you could have left some remarks about it out (such as the statement I quoted) without taking away from the actual points you were making. <br /><br /> Ehttps://www.blogger.com/profile/01258284747813821500noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-37134517513802811532014-03-25T22:25:08.025-07:002014-03-25T22:25:08.025-07:00Jason's comments are more in line with what I ...Jason's comments are more in line with what I learned at UIUC as an Animal Science major while taking Animal Reproduction, Lactation, and Growth. While we were talking farm animals, the same principles apply. From my recollection, artificial hormones work primarily on the biofeedback loop, preventing the appropriate levels of natural hormone production (estrogen and progesterone). Without sufficient estrogen, the uterine lining does not develop sufficiently, even if progesterone is not blocked. I'd recommend you delve into animal science research if you are looking for greater detail. They can (and do) experiment with animals in ways not possible with humans, that is, they can apply the hormones, then slaughter the animals and measure the organs. (The experiment we did with mice, with estrogen, progesterone, and both, was such an experiment.)<br /><br />The original human contraceptives were more effective at preventing pregnancy, as the levels of estrogen were higher and less break-through ovulations occurred, but that came at a steep price in women dying in greater numbers from blood clots and strokes. Even if you cling to the possibility that hormonal contraceptives don't abort a newly conceived child, why would you want to subject yourself (if you're a woman) or the woman you love to powerful hormones that are known to cause breast cancer (WHO 2005, NIH 2007), heart disease, strokes, and death, among other harms? Especially when modern Natural Family Planning is available for spacing or avoiding pregnancy if a serious reason exists? NFP is 100% safe for mothers and babies, over 99% effective when used correctly, and builds relationships through communication. The Couple to Couple League has more information.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-31657987631596001042013-11-15T07:47:22.817-08:002013-11-15T07:47:22.817-08:00I just recently found this post. Do you have any ...I just recently found this post. Do you have any updates that would either strengthen or weaken your case?Drewhttps://www.blogger.com/profile/03178352431939269649noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-61184928419287575092012-10-14T23:48:50.546-07:002012-10-14T23:48:50.546-07:00Heу! Thіs is kind of off topic but I neеd some
hе...Heу! Thіs is kind of off topic but I neеd some <br />hеlp fгom an established blοg.<br />Is іt hard to set up your οwn blog? I'm not very techincal but I can figure things out pretty quick. I'm thinkіng аbout creating my own but I'm not sure where to start. Do you have any ideas or suggestions? Cheers<br /><i>my web site</i> - <b><a href="http://Cort.as/2EbR" rel="nofollow">cort.as</a></b>Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-17535373135377295902012-01-12T17:43:05.012-08:002012-01-12T17:43:05.012-08:00I've provided some links on this subject in a ...I've provided some links on this subject in a June entry in my blog, which you can find a link to in my name. I've also commented on this subject in a couple of December entries and a few others.Robert Treathttps://www.blogger.com/profile/15105712543056686717noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-92157747554286204452010-03-07T23:16:28.719-08:002010-03-07T23:16:28.719-08:00Are there any peer reviewed articles on this subje...Are there any peer reviewed articles on this subject yet, or any 2009 or 2010 information? I'm really looking into this issue... So far, this is one of the most helpful resources I have found. Does anyone know of any more recent info?Kevinnoreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-46134115106227236552008-07-04T05:48:00.000-07:002008-07-04T05:48:00.000-07:00"{I}t’s my understanding that breakthrough ovulati..."{I}t’s my understanding that breakthrough ovulation does not occur because the natural body processes were able to “override” the pill, but because the pill was not used properly, and in the absence of its hormonal regiment, the normal cycle processes resumed. And if it is just the normal process resuming, I see no reason to think the body will produce “catch-up” estrogen to try to normalize the endometrium by the time of ovulation."<BR/><BR/>Several points are relevant here. First of all, if breakthrough ovulation occurs _only_ when the pill is used improperly, this hardly should be a major conscience problem, or perhaps any conscience problem at all, *in and of itself*, to a conscientious Christian woman using the pill. For she is not a careless person and is intending to use the pill properly. Moreover, other methods can be used as back-up if she misses a single pill. It's hardly fair to say "the pill kills" if one means "the pill kills (or might kill) when you don't use it the way you are supposed to." In the paper I linked in Serge's other thread, which I _highly recommend_, by the AAPLOG guys, they expressly use only the known pregnancy rate of the pill with compliant users for their calculations. This seems only fair.<BR/><BR/>Second of all, you speak about the "normal processes" resuming. But I think it's very important to understand that, as a part of a normal process, ovulation does not occur for no reason. The hormonal cascade necessary to cause ovulation is rather precise. If there isn't estrogen, and a lot of it, there isn't the LH surge. And if there isn't a good bit of estrogen, the cervical mucus is not receptive, and conception cannot take place. If there isn't FSH, then no follicle gets to the point of being ready to burst out when the LH surge comes. But FSH causes the body to produce more estrogen, etc.<BR/><BR/>Now, that _is_ the normal process. I get the impression that you know that, but in that case, it seems that there is something to my point that even if one were to miss a pill or, with perfect compliance, the ovaries were to ovulate despite the pill, there would *have to be* significant quantities of estrogen and FSH in the system prior to ovulation, or else ovulation simply wouldn't happen. It's not literally impossible, I suppose, that a brief and sky-high spike of estrogen--say, for just one or two days prior to ovulation--should produce all the effects necessary for ovulation, but even that would (I would think) produce some pre-ovulatory endometrial thickening, more so than in a cycle where ovulation was not going to occur and the ovaries were responding fully to the pill. Moreover, it seems to be an open question whether only one or two days' worth of estrogen and FSH _all by itself_ would be enough to bring about ovulation. It isn't usually enough, as far as I can tell. The normal cycle involves about 7 days post-menstruation of stimulation of the ovaries by FSH and of increasing amounts of estrogen before ovulation occurs at all. These things are _causal_ for ovulation, and they are also _causal_ for endometrial thickening. It wouldn't be a matter of the body's "trying to catch up" but rather of the fact that hormonal events pre-ovulation that produce endometrial thickening--specifically, the presence of lots of estrogen--also produce ovulation.<BR/><BR/>I think an easy mistake to fall into here is to treat all of these physical events as causally independent so that one then uses a faulty "all else being equal" assumption. "Suppose ovulation occurs, all else being equal." Well, for one thing, if that _were_ possible, the cervical mucus would be totally unreceptive, and you wouldn't have to worry about fertilization! But then, it's as though one is trying to _create_ a worry. "Suppose ovulation occurred, and there were _just enough_ estrogen in the system prior to ovulation to prepare receptive cervical mucus, but there had been _just too little_ estrogen in the system prior to ovulation to thicken the endometrium, and even though all the luteal phase thickening and preparation occurred, that pre-ovulatory difference were just enough to prevent implantation."<BR/><BR/>This seems to me, given the causal interconnectedness of the events involved, like an artificial worry from an empirical perspective.Lydia McGrewhttps://www.blogger.com/profile/00423567323116960820noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-53808377290516398752008-07-02T11:16:00.000-07:002008-07-02T11:16:00.000-07:00Lydia,That explanation makes sense, which makes me...Lydia,<BR/><BR/>That explanation makes sense, which makes me question all the more whether they are talking about the thickness of the endometrium. It is one thing to say that the baloons in group X are larger than those in group Y, but a wholly other matter to say the baloons in group X are thicker than the baloons in group Y. Are they talking about size or thickness? <BR/><BR/>Clearly they are talking about size in the first sentence, but are they doing so in the second when they speak of endometrial "growth?" If not, then this quote does not pertain to the issue I raised after all, and there is nothing in the paper that would deem the notion that the pill causes a thin endometrium.<BR/><BR/>I am inclined to think they are referring to endometrial thickness, because earlier in the paper they used "growth" to refer to thickness. And yet, by starting off with "indeed," the second sentence seems to be an expansion on the point of the first sentence, which is about the size of the uterus, not the thickness of its wall. That makes me think this entire paragraph is about how the pill affects the size of the uterus, not the endometrium. I am hoping Serge can shed some more light on this.Jason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-61463968419954137982008-07-02T11:06:00.000-07:002008-07-02T11:06:00.000-07:00I’m not Serge, but I did want to interact with som...I’m not Serge, but I did want to interact with some of what you said. <BR/><BR/>Regarding your 2nd paragraph in your 1st post, it is true that most of the thickness of the endometrium has been built up by the time of ovulation. It continues to be built in the luteal phase, as estrogen continues to be present. Progesterone also increases to the thickness. From what I have read it induces swelling, and increases secretion by stimulating glands in the endometrium, making it spongy and strong. I like to think of the process as water being applied to a very dry sponge. A dry sponge is porous, but stiff and of no use for cleaning. But once water is applied, it thickens up, and becomes receptive to gook. In a similar fashion, estrogen builds the sponge, but progesterone hydrates it (and just like the sponge, the endometrium expands when “hydrated” by the secretory fluids).<BR/><BR/>Regarding your 3rd paragraph in your 1st post, your suggestion is plausible. To stick with my analogy, even a very thin sponge, when hydrated, can clean up gook. It just doesn’t do it as well as a thicker sponge. Maybe the same is true of the endometrium. Then again, maybe not. Maybe it is like seed in soil. Seed grows best in deep soil. While some seed manage to grow in well-watered, shallow soil, some cannot take root. Likewise, it could be that the endometrium is too “shallow” for the embryo to “take root,” even though it is “well watered.” I don’t know. I’m just bringing up possibilities.<BR/><BR/>Regarding your final paragraph, it’s my understanding that breakthrough ovulation does not occur because the natural body processes were able to “override” the pill, but because the pill was not used properly, and in the absence of its hormonal regiment, the normal cycle processes resumed. And if it is just the normal process resuming, I see no reason to think the body will produce “catch-up” estrogen to try to normalize the endometrium by the time of ovulation.Jason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-66781585064141038052008-07-01T19:52:00.000-07:002008-07-01T19:52:00.000-07:00Jason, I think the reason they are mentioning past...Jason, I think the reason they are mentioning past history of pregnancy is because they are measuring overall uterus size, which would be affected by past pregnancy. One of their speculations is that the women on the pill had smaller uteri because the uterus apparently gets bigger with increased estrogen during the cycle, but pill users would have less estrogen in their systems. But I think they are saying that they couldn't get a good comparison sample that allowed them to "control" for the effect of past pregnancy on overall uterus size. In other words, it might be that the women on the pill had, on average, smaller uteri simply because most of them had never been pregnant before.<BR/><BR/>There is, of course, no question that women taking the pill have less estrogen in their systems than women not taking the pill. The major question for purposes of this discussion, however, is whether that is true only, or only to any significant extent, for women on the pill *who do not ovulate* and whether breakthrough ovulation would give us an entirely different sample group with an entirely different endometrial profile.Lydia McGrewhttps://www.blogger.com/profile/00423567323116960820noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-38416584913180720422008-07-01T19:41:00.000-07:002008-07-01T19:41:00.000-07:00Serge, can you give quickly the source citation fo...Serge, can you give quickly the source citation for your great chart here of all the occurrences in the cycle? I'm writing something up on this for my own use and want to print out the entry, including the chart, and give the source for the chart.<BR/><BR/>It's interesting for me to see as I look up some other sources that it appears fairly common for popular-level writing on this subject to imply quite explicitly that the _thickness_ of the endometrium is determined _before_ ovulation. For example, I have a book called _How to Get Pregnant_ that says pretty much exactly that. The author states that the corpus luteum causes the endometrium to become "spongy" and receptive but says that the thickness is built up (he implies, entirely) prior to ovulation by the estrogen in the woman's system during the follicular phase. This obviously is incorrect.<BR/><BR/>An interesting point in response to some of the considerations Jason is raising is this: If the corpus luteum makes a significant increase in the thickness endometrium in a case of break-through ovulation (which we can assume it would do), and if it also makes the endometrium more receptive in other ways (which we can assume it would do), how plausible is it that implantation would be prevented entirely by a somewhat different "start point" for that thickening process? Even if the final thickness were not as great as for a woman not taking OC's, do we have reason to think that a significantly thickened and otherwise receptive endometrium would in fact be "hostile" to implantation?<BR/><BR/>Another point: If breakthrough ovulation occurs, presumably it occurs because of some hormonal events before ovulation. Perhaps only a couple of days before, but nonetheless, breakthrough ovulation doesn't occur by magic or for no hormonal reason. Is there not reason to think that the very hormonal causes that permitted breakthrough ovulation--the body's "overriding" the pill to that extent--would also result in a higher release of estrogen in the days prior to ovulation and hence in a thicker endometrium even at the time of ovulation than one finds in the typical, non-ovulatory, woman using the pill?Lydia McGrewhttps://www.blogger.com/profile/00423567323116960820noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-32481297988371112962008-07-01T12:30:00.000-07:002008-07-01T12:30:00.000-07:00Serge,Yes, the 1.1mm figure is an average thicknes...Serge,<BR/><BR/>Yes, the 1.1mm figure is an average thickness, but the authors do state: “Endometnial thickness was not significantly different between the follicular and secretory phases in the pill-using group; whereas in the nonpill group, the endometnium was significantly larger (P < .025) in the secretory than in the follicular phase.” It seems, then, that the data on which I based my concern is correct. <BR/><BR/>Regarding the portion of the paper you quoted, the full quote is as follows: “Prolonged use of the pill can cause a decrease in corpus size, perhaps accounting for the smaller size of the uteri in the pill-using group in the follicular phase. Indeed, the combination pill may obliterate the uterine growth that occurs with increasing estrogen titers in the follicular phase. However, since there were fewer parous women in the pill-using group than in the nonpill group, this explanation is somewhat speculative.”<BR/><BR/>Questions:<BR/>1. In the first sentence, do they mean the uterus itself is smaller, or the thickness of the endometrium? It seems to me that they are saying the pill shrinks the uterus, but the second sentence seems to be speaking of endometrial thickness.<BR/>2. How could a past pregnancy affect how the pill works? It seems to me that the pill would suppress estrogen production (and thus endometrial growth in the follicular phase) in every woman, regardless of her childbearing history. <BR/><BR/>I think we should also be clear on what they are speculating about. They are speculating that the reason the endometrium is only 1mm thick in pill users is because the pill suppresses estrogen production. They are not speculating that the pill is responsible for keeping the endometrium at 1mm thickness. As they write, “Endometrial thickness was significantly smaller in the pill-using group, correlating with the well-established fact that oral contraceptives cause atrophy of the endometrium.” Indeed, earlier in the paper they are clear that “as the estrogen level rises due to follicular growth, the endometrium thickens.” If that is why the endometrium thickens in non-pill users, I don’t think it is very speculative to think that the endometrium is thin in pill users because the pill interferes with estrogen production.<BR/><BR/>What are your thoughts?<BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-38797204008201292212008-06-30T09:12:00.000-07:002008-06-30T09:12:00.000-07:00This has been a really good. To close a loop in m...This has been a really good. To close a loop in my mind, is it possible for someone to comment on differences between what is mentioned here and 'Emergency Contraception'.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-73595771040296731932008-06-26T14:24:00.000-07:002008-06-26T14:24:00.000-07:00That was easier than I thought. I was able to vie...That was easier than I thought. I was able to view the full article here (http://radiology.rsnajnls.org/cgi/reprint/160/1/119)<BR/><BR/>The number did not change because they are mean values. They did not distinguish between the different days of the cycle, but only characterized the 21 women in the study as in either the follicular or the secretory (luteal) phase.<BR/><BR/>Even more interesting, the author states that the pill may change the lining in the follicular phase, but follows it with this sentence:<BR/><BR/>"However, since there were fewer parous women in the pill-using group than in the non-pill group, this explanation is somewhat speculative".Serge (Rich Poupard)https://www.blogger.com/profile/06648112986475922045noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-33964479346377811912008-06-26T14:00:00.000-07:002008-06-26T14:00:00.000-07:00Jason,I have much to say but time is short today. ...Jason,<BR/><BR/>I have much to say but time is short today. Here is the abstract of the study you cited:<BR/><BR/>"Magnetic resonance (MR) imaging was performed on 21 women in different phases of the menstrual cycle, nine who used oral contraceptives and 12 who did not. Sagittal images in a dual spin-echo sequence were obtained to assess conspicuity and dimensions of the corpus uteri, cervix, vagina, and their component tissues. The endometrium, junctional zone, myometrium, cervical canal, fibrous stroma, and vaginal canal were seen in all cases and the vesicovaginal septum, rectovaginal septum, and levator ani in 90%, 86%, and 100%, respectively. The uterus was retrodisplaced in 19% of the women. In the nonpill group, endometrial width was significantly larger (P less than .025) in the secretory phase (mean, 5 mm) than in the follicular phase (3.1 mm). In the pill-using group, endometrial width was 1.1 mm in both phases, significantly smaller than in the nonpill group (P less than .025, follicular; P less than .0005, secretory). Junctional zone width was significantly smaller in the pill-using group (P less than .005). Qualitatively, the myometrium was relatively brighter on second echo images in the pill-using group, compatible with known edema that occurs with use of oral contraceptives. MR can reliably demonstrate gynecologic structure and anatomic changes that occur during the menstrual cycle and with use of oral contraceptives."<BR/><BR/>There are two questions I have here. First, as you know the uterine lining changes at different points in the follicular phase (although not as much as the luteal phase). Where in the cycle was the 1.1mm figure taken, and how was that determined?<BR/><BR/>Secondly, how is it even possible that the uterine lining did not change at all in these 10 women throughout the cycle? Assuming that they menstruated, why was there not some variation in uterine thickness?<BR/><BR/>I may try to pick up the original paper when I get a chance.Serge (Rich Poupard)https://www.blogger.com/profile/06648112986475922045noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-52966245701609405742008-06-26T13:14:00.000-07:002008-06-26T13:14:00.000-07:00Jay,I would agree that Serge comes off as anti-ove...Jay,<BR/><BR/>I would agree that Serge comes off as anti-overstatement (rightly so), but a little less pro-caution. I think I have my foot on the brakes a little more than him, but for good reason. He is pretty confident that the Pill poses no abortifacient risk to an embryo, and that if it does, it is as negligible as other standard medical risks, and thus does not warrant total abstention. The more one is confident of this, the less reason there is for them to caution people against using the Pill. Indeed, if he is able to show me that my concerns about the development of the endometrium in the follicular phase are medically invalid, I'm sure my pro-caution advocacy will be turned down a few notches as well. <BR/><BR/>I agree with you about the quality of the dialogue here. Not only is it civil, but it has remained on point, and is helping people to better understand the issues, and sort out the truth. I would like to say publicly how invaluable I find Serge's knowledge in this area to be, and how happy I am to have him interact with me on this topic. It's not an easy thing to sort out, and I appreciate the time he has taken to do so.<BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-46783355602815430862008-06-25T18:55:00.001-07:002008-06-25T18:55:00.001-07:00This comment has been removed by the author.Jay Wattshttps://www.blogger.com/profile/11298001988620531769noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-54389735031120107112008-06-25T18:55:00.000-07:002008-06-25T18:55:00.000-07:00Jason,My mentioning Serge's caution was to counter...Jason,<BR/><BR/>My mentioning Serge's caution was to counter the sense that Serge is pro-pill or anti-pill and to highlight that he is pro caution and anti overstatement. <BR/><BR/>If I connected Serge in some way to a sentiment that he does not endorse by accident then I apologize.<BR/><BR/>I want to say that I personally love this thread and it is this type of exchange that restores my faith in the value of comment threads.<BR/><BR/>God bless,<BR/>JayJay Wattshttps://www.blogger.com/profile/11298001988620531769noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-21923962949952609182008-06-25T17:44:00.000-07:002008-06-25T17:44:00.000-07:00Serge,I looked at Larimore's paper again. The mos...Serge,<BR/><BR/>I looked at Larimore's paper again. The most immediate reference is to one of his own papers, found at http://archfami.ama-assn.org/cgi/content/full/9/2/126?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Postfertilization+effects+of+oral+contraceptives+and+their+relationship+to+informed+consent&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT#REF-FSA8035-50.<BR/><BR/>When I went there, this was his reference for the claim that the endometrium is only 1.1mm thick for women on the Pill: McCarthy S, Tauber C, Gore J. Female pelvic anatomy: MR assessment of variations during the menstrual cycle and with use of oral contraceptives. Radiology. 1986;160:119-123. He provides a link to this study: http://radiology.rsnajnls.org/cgi/content/abstract/160/1/119?ijkey=ef9f223a35051ddb173cd72c06fddc68547629cd&keytype2=tf_ipsecsha<BR/><BR/>Check it out and tell me what you think. Thanks!<BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-48834710086083450532008-06-25T17:33:00.000-07:002008-06-25T17:33:00.000-07:00Jay,Serge can correct me, but it is my understandi...Jay,<BR/><BR/>Serge can correct me, but it is my understanding that he thinks it best to avoid the Pill, but not because of its supposed potential abortifacient effects. In the comments section of his prior post he wrote, "I actually think it may be advisable to eschew the pill regardless of whether or not it causes a hostile endometrium. However, since I believe that the likelihood of the pill causing an embryo to fail to implant is extremely small and may be zero, I would not use the potential impact on the endometrium as a sole basis to avoid the pill." I, in contrast, think a possible abortifacient effect of the Pill alone is sufficient to advise people to eschew the Pill (although there are other health-related reasons to do so as well). <BR/><BR/>But I also agree with you and Serge that we should not overstate our case. We cannot claim the Pill does have an abortifacient effect, but only that it might.<BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-62384104007709731062008-06-24T07:56:00.000-07:002008-06-24T07:56:00.000-07:00Jason,I certainly agree with Jay's comments. Your...Jason,<BR/><BR/>I certainly agree with Jay's comments. Your thoughtful investigation into this issue is refreshing.<BR/><BR/>Your citation of Stanford can be found here (http://www.aafcp.org/files/sci_res_forum95.pdf), and no mention of endometrial thickness is in that abstract. I am not having an easy time finding a paper that investigates the endometrial thickness in the late follicular phase for women taking OCs. It would be a very good study to perform (and shouldn't be very difficult.) Since the thickness varies throughout the cycle, the time that the US examination is performed is essential.<BR/><BR/>In looking at the effect at FSH and estrogen levels in the follicular phase - it seems clear that women on OCs have less FSH and estrogen, but certainly not zero. I will concede that it is reasonable to believe that this has some effect on the endometrial thickness in the follicular phase, but not to the extent that you state. <BR/><BR/>Lastly, most investigators point to the endometrial changes in the luteal phase as being by far the most essential aspect of preparing the endometrium for accepting an embryo. Its not merely a matter of endometrial thickness, but a host of changes that appear necessary (at least most of the time) for the uterine lining to accept an embryo. <BR/><BR/>In short, I have stated and still do that I cannot prove that OCs do not impair the ability to the uterine lining to accept an embryo. I am not convinced, but reasonable persons (such as yourself) disagree with me. <BR/><BR/>The problem that I have are those who believe this issue is a settled one. Overstating our case does nothing to help us. I applaud you for not doing so.Serge (Rich Poupard)https://www.blogger.com/profile/06648112986475922045noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-26852143502267424182008-06-23T05:52:00.000-07:002008-06-23T05:52:00.000-07:00Jason,I was quite confident in what you meant. I ...Jason,<BR/><BR/>I was quite confident in what you meant. I wanted to be certain that what I knew was clear to anyone less familiar with all of this than you. It was a clarification comment.<BR/><BR/>I think it is important to point out that Serge has said that he thinks that using OC's is probably not a good idea. His original object, and my continued objection, is to those who say "the Pill Kills," and then campaign against OC's as if this question was settled. That is overstating the case.<BR/><BR/>We need to educate people as to why we ought to consider the effects of oral contraceptives. On a personal note, my wife and I stopped using OC's after reading a little about it. We cannot claim that we know that OC's kill babies and be operating in a spirit of honesty. Worse than fear mongering, it is distracting dishonest fear mongering. That never seems the right tactic for those objecting on moral principles.<BR/><BR/>Your objections and thoughtful considerations are a far cry from that.Jay Wattshttps://www.blogger.com/profile/11298001988620531769noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-74818517448661501662008-06-20T11:47:00.000-07:002008-06-20T11:47:00.000-07:00Jay,I would agree with everything you said, but I ...Jay,<BR/><BR/>I would agree with everything you said, but I stand by my comments at the same time. While I agree with you that the pro-abortion objection is based in ignorance, one of the pro-life responses to the objection shows that even if we assume this were true, it does not argue for abortion, but against it, based on the principle that we should err on the side of life. <BR/><BR/>My point was that this same principle should inform our decision to use the Pill. Beyond that, there is no 1:1 analogy between the two issues. As you pointed out, in the case of abortion we know something is being killed but are uncertain as to whether that thing has value. In the case of the Pill, we are both uncertain if anything is being killed, and if something is, whether that thing has value. All this shows is that we are less certain about the morality of taking the Pill than we are about the morality of abortion. It doesn’t mean we should not equally err on the side of life, due to our ignorance of the answers to these decisive questions. <BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.comtag:blogger.com,1999:blog-1442827238174603755.post-68703256878225202092008-06-20T11:23:00.000-07:002008-06-20T11:23:00.000-07:00Serge,Thanks for your quick response to my tome.Yo...Serge,<BR/><BR/>Thanks for your quick response to my tome.<BR/><BR/>You asked if I “have evidence that FSH is effected to that level, and that the ovaries fail to produce any estrogen during the follicular phase.” My evidence would be the result: a 1.1mm thick endometrium. I got this figure from Walter Larimore’s paper, “The Growing Debate About the Abortifacient Effect of the Birth Control Pill and the Principle of the Double Effect.” He cited MRI studies for this figure, referencing Stanford JB, Daly KD. Menstrual and mucus cycle characteristics in women discontinuing oral contraceptives (abstract). Paediatr Perinat Epidemiol 1995;9(4): A9.. Is that info wrong? It is important to my case, so if it is wrong, much of my doubt in this area can be resolved.<BR/><BR/>For your specific points:<BR/><BR/>(1) If a mature follicle is 15mm, and some women on the Pill have follicles that reach 10mm, we might infer that FSH levels can reach a max of 2/3 their norm, and that the ovaries in turn produce 2/3 their normal amount of estrogen. If so, then the 5-8mm of endometrium estrogen normally builds would be about 2-3mm in Pill users, rather than 1mm as cited by Larimore. But how much estrogen is released by the follicle itself, separate from the ovaries? At http://www.healthsquare.com/fgwh/wh1ch17.htm I read that the mature follicle produces a lot of estrogen. Could it be that since no follicle fully matures, estrogen production never reaches its normal potential, keeping the endometrium to 1mm thick? <BR/><BR/>(2) I acknowledged this in my comments. But their flow is light, because the endometrium did not experience much thickening (but it did get to 1mm or so, again, assuming that figure is accurate).<BR/><BR/>(3) One of my sources was http://sprojects.mmi.mcgill.ca/menstrualcycle/endocrinology.html. There may have been others as well, but that’s the only reference I had in my notes. If the presence of FSH in the ovaries is not what stimulates them to produce estrogen, then what stimulates estrogen production?<BR/><BR/>JasonJason Dullehttps://www.blogger.com/profile/16840891072959191210noreply@blogger.com